Evidence map›Paper›PMID 28219902›Full record

ArticleEMBO reports2017

NDR1 protein kinase promotes IL-17- and TNF-α-mediated inflammation by competitively binding TRAF3.

Chunmei Ma, Wenlong Lin, Zhiyong Liu, Wei Tang, Rahul Gautam, Hui Li, Youcun Qian, He Huang, Xiaojian Wang

Open access · greenAbstract read
In one paragraph

Article in EMBO reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 48 citations in OpenAlex.

  1. DYRK kinases phosphorylate IL-17RA at S801.Serican journal of medicine · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. The NDR family of kinases: essential regulators of aging.Frontiers in molecular neuroscience · 2024
    Review
  8. Role of TBK1 Inhibition in Targeted Therapy of Cancer.Mini reviews in medicinal chemistry · 2024
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Epac-2 ameliorates spontaneous colitis in Il-10Journal of cellular and molecular medicine · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Chunmei MaInstitute of Immunology, School of Medicine, Zhejiang University, Hangzhou, China.
Wenlong LinInstitute of Immunology, School of Medicine, Zhejiang University, Hangzhou, China.
Zhiyong LiuInstitute of Immunology, School of Medicine, Zhejiang University, Hangzhou, China.
Wei TangInstitute of Immunology, School of Medicine, Zhejiang University, Hangzhou, China.
Rahul GautamInstitute of Immunology, School of Medicine, Zhejiang University, Hangzhou, China.
Hui LiDepartment of Chemotherapy, Zhejiang Cancer Hospital, Hangzhou, China.
Youcun QianStem Cell Biology, Institute of Health Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine, Shanghai, China.
He HuangBone Marrow Transplantation Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Xiaojian WangInstitute of Immunology, School of Medicine, Zhejiang University, Hangzhou, China wangxiaojian@cad.zju.edu.cn.ORCID 0000-0001-8232-0558
Zhejiang University · CNFirst Affiliated Hospital Zhejiang University · CNShanghai Jiao Tong University · CNZhejiang Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin 17 (IL-17) is an important inducer of tissue inflammation and is involved in numerous autoimmune diseases. However, how its signal transduction is regulated is not well understood. Here, we report that nuclear Dbf2-related kinase 1 (NDR1) functions as a positive regulator of IL-17 signal transduction and IL-17-induced inflammation. NDR1 deficiency or knockdown inhibits the IL-17-induced phosphorylation of p38, ERK1/2, and p65 and the expression of chemokines and cytokines, whereas the overexpression of NDR1 promotes IL-17-induced signaling independent of its kinase activity. Mechanistically, NDR1 interacts with TRAF3 and prevents its binding to IL-17R, which promotes the formation of an IL-17R-Act1-TRAF6 complex and downstream signaling. Consistent with this, IL-17-induced inflammation is significantly reduced in

Indexed as

AnimalsCell LineColitisCytokinesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalHumansInflammationInflammation MediatorsInterleukin-17Mice, KnockoutProtein BindingProtein Serine-Threonine KinasesSignal TransductionTNF Receptor-Associated Factor 3Tumor Necrosis Factor-alphaCytokinesInflammation MediatorsInterleukin-17NDR1 protein kinase, mouseProtein Serine-Threonine KinasesTNF Receptor-Associated Factor 3Tumor Necrosis Factor-alphaIL‐17inflammationNDR1TRAF3

Identifiers

PMID28219902
PMCPMC5376972
OpenAlexW2589236405

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.